Enables several functions, including amino acid binding activity; amyloid-beta binding activity; and monoatomic ion gated channel activity. Involved in several processes, including modulation of chemical synaptic transmission; positive regulation of dendritic spine maintenance; and protein heterotetramerization. Located in several cellular components, including dendrite; postsynaptic density; and synaptic cleft. Part of NMDA selective glutamate receptor complex. Is active in several cellular components, including hippocampal mossy fiber to CA3 synapse; parallel fiber to Purkinje cell synapse; and synaptic membrane. Biomarker of cognitive disorder; middle cerebral artery infarction; placental insufficiency; sciatic neuropathy; and status epilepticus. Human ortholog(s) of this gene implicated in alcohol use disorder; autosomal dominant intellectual developmental disorder 8; cerebral infarction; and developmental and epileptic encephalopathy. Orthologous to human GRIN1 (glutamate ionotropic receptor NMDA type subunit 1); PARTICIPATES IN excitatory synaptic transmission pathway; alfentanil pharmacodynamics pathway; bupivacaine pharmacodynamics pathway; INTERACTS WITH (+)-pilocarpine; (25R)-cholest-5-ene-3beta,26-diol; (R)-lipoic acid.
Thioctic Acid inhibits the reaction [methylmercuric chloride results in decreased expression of GRIN1 mRNA], Thioctic Acid inhibits the reaction [methylmercuric chloride results in decreased expression of GRIN1 protein]
[[Lithium Chloride co-treated with Estradiol] results in decreased expression of GRIN1 mRNA] which affects the susceptibility to Excitatory Amino Acid Agonists, [Lithium Chloride co-treated with Estradiol] results in decreased expression of GRIN1 mRNA
fulvestrant inhibits the reaction [estradiol 3-benzoate results in increased phosphorylation of GRIN1 protein], U 0126 inhibits the reaction [estradiol 3-benzoate results in increased phosphorylation of GRIN1 protein]
[BDNF protein co-treated with GDNF protein co-treated with Cyclic AMP co-treated with TGFB3 protein co-treated with Ascorbic Acid] results in increased expression of GRIN1 mRNA
[SN50 peptide affects the localization of [RELA protein binds to NFKB1 protein]] inhibits the reaction [Tretinoin results in increased expression of GRIN1 protein]
agomelatine inhibits the reaction [Galactose results in increased expression of GRIN1 protein], Melatonin inhibits the reaction [Galactose results in increased expression of GRIN1 protein]
[bisphenol A co-treated with enzacamene co-treated with octylmethoxycinnamate co-treated with butylparaben co-treated with Androgen Antagonists co-treated with Acetaminophen] results in increased expression of GRIN1 mRNA
[Dibutyl Phthalate co-treated with Diethylhexyl Phthalate co-treated with vinclozolin co-treated with prochloraz co-treated with procymidone co-treated with Linuron co-treated with epoxiconazole co-treated with Dichlorodiphenyl Dichloroethylene] results in increased expression of GRIN1 mRNA
[bisphenol A co-treated with enzacamene co-treated with octylmethoxycinnamate co-treated with butylparaben co-treated with Androgen Antagonists co-treated with Acetaminophen] results in increased expression of GRIN1 mRNA more ...
[bisphenol A co-treated with enzacamene co-treated with octylmethoxycinnamate co-treated with butylparaben co-treated with Androgen Antagonists co-treated with Acetaminophen] results in increased expression of GRIN1 mRNA, [bisphenol A co-treated with enzacamene co-treated with octylmethoxycinnamate co-treated with butylparaben] results in increased expression of GRIN1 mRNA
Choline analog inhibits the reaction [lead acetate results in decreased expression of GRIN1 mRNA], Choline analog inhibits the reaction [lead acetate results in decreased expression of GRIN1 protein]
[Dibutyl Phthalate co-treated with Diethylhexyl Phthalate co-treated with vinclozolin co-treated with prochloraz co-treated with procymidone co-treated with Linuron co-treated with epoxiconazole co-treated with Dichlorodiphenyl Dichloroethylene] results in increased expression of GRIN1 mRNA
[Dibutyl Phthalate co-treated with Diethylhexyl Phthalate co-treated with vinclozolin co-treated with prochloraz co-treated with procymidone co-treated with Linuron co-treated with epoxiconazole co-treated with Dichlorodiphenyl Dichloroethylene] results in increased expression of GRIN1 mRNA
[Dopamine results in increased activity of DRD1 protein] which results in increased phosphorylation of GRIN1 protein, N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide inhibits the reaction [[Dopamine results in increased activity of DRD1 protein] which results in increased phosphorylation of GRIN1 protein]
[bisphenol A co-treated with enzacamene co-treated with octylmethoxycinnamate co-treated with butylparaben co-treated with Androgen Antagonists co-treated with Acetaminophen] results in increased expression of GRIN1 mRNA, [bisphenol A co-treated with enzacamene co-treated with octylmethoxycinnamate co-treated with butylparaben] results in increased expression of GRIN1 mRNA
[Dibutyl Phthalate co-treated with Diethylhexyl Phthalate co-treated with vinclozolin co-treated with prochloraz co-treated with procymidone co-treated with Linuron co-treated with epoxiconazole co-treated with Dichlorodiphenyl Dichloroethylene] results in increased expression of GRIN1 mRNA
[[Lithium Chloride co-treated with Estradiol] results in decreased expression of GRIN1 mRNA] which affects the susceptibility to Excitatory Amino Acid Agonists
fluorocitrate inhibits the reaction [Biological Factors results in increased expression of GRIN1 mRNA], fluorocitrate inhibits the reaction [Biological Factors results in increased expression of GRIN1 protein]
fulvestrant inhibits the reaction [bisphenol A results in increased phosphorylation of GRIN1 protein], fulvestrant inhibits the reaction [estradiol 3-benzoate results in increased phosphorylation of GRIN1 protein]
agomelatine inhibits the reaction [Galactose results in increased expression of GRIN1 protein], Melatonin inhibits the reaction [Galactose results in increased expression of GRIN1 protein]
[BDNF protein co-treated with GDNF protein co-treated with Cyclic AMP co-treated with TGFB3 protein co-treated with Ascorbic Acid] results in increased expression of GRIN1 mRNA
[Dibutyl Phthalate co-treated with Diethylhexyl Phthalate co-treated with vinclozolin co-treated with prochloraz co-treated with procymidone co-treated with Linuron co-treated with epoxiconazole co-treated with Dichlorodiphenyl Dichloroethylene] results in increased expression of GRIN1 mRNA
Thioctic Acid inhibits the reaction [methylmercuric chloride results in decreased expression of GRIN1 mRNA], Thioctic Acid inhibits the reaction [methylmercuric chloride results in decreased expression of GRIN1 protein]
[Particulate Matter co-treated with lipoteichoic acid] results in increased expression of GRIN1 mRNA, [Vehicle Emissions co-treated with lipoteichoic acid] results in increased expression of GRIN1 mRNA
[[Lithium Chloride co-treated with Estradiol] results in decreased expression of GRIN1 mRNA] which affects the susceptibility to Excitatory Amino Acid Agonists, [Lithium Chloride co-treated with Estradiol] results in decreased expression of GRIN1 mRNA
[Morphine results in increased activity of OPRM1 protein] which results in increased phosphorylation of GRIN1 protein, MMP9 protein affects the reaction [Morphine results in increased phosphorylation of GRIN1 protein]
[[Ozone results in increased oxidation of Particulate Matter] which results in increased chemical synthesis of Aerosols] which results in increased expression of GRIN1 mRNA, [[Ozone results in increased oxidation of Vehicle Emissions] which results in increased chemical synthesis of Aerosols] which results in increased expression of GRIN1 mRNA
[bisphenol A co-treated with enzacamene co-treated with octylmethoxycinnamate co-treated with butylparaben co-treated with Androgen Antagonists co-treated with Acetaminophen] results in increased expression of GRIN1 mRNA
[Dibutyl Phthalate co-treated with Diethylhexyl Phthalate co-treated with vinclozolin co-treated with prochloraz co-treated with procymidone co-treated with Linuron co-treated with epoxiconazole co-treated with Dichlorodiphenyl Dichloroethylene] results in increased expression of GRIN1 mRNA
[Dibutyl Phthalate co-treated with Diethylhexyl Phthalate co-treated with vinclozolin co-treated with prochloraz co-treated with procymidone co-treated with Linuron co-treated with epoxiconazole co-treated with Dichlorodiphenyl Dichloroethylene] results in increased expression of GRIN1 mRNA
resveratrol inhibits the reaction [Morphine results in increased expression of [GRIN1 protein binds to GRIN2B protein binds to DLG4 protein]], resveratrol inhibits the reaction [Morphine results in increased expression of GRIN1 protein]
Curcumin inhibits the reaction [sodium arsenite results in decreased expression of GRIN1 mRNA], Curcumin inhibits the reaction [sodium arsenite results in decreased expression of GRIN1 protein]
[Dibutyl Phthalate co-treated with Diethylhexyl Phthalate co-treated with vinclozolin co-treated with prochloraz co-treated with procymidone co-treated with Linuron co-treated with epoxiconazole co-treated with Dichlorodiphenyl Dichloroethylene] results in increased expression of GRIN1 mRNA
Molecular characterization of N-methyl-D-aspartate receptors expressed in mammalian cells yields evidence for the coexistence of three subunit types within a discrete receptor molecule.
Abeta oligomers induce neuronal oxidative stress through an N-methyl-D-aspartate receptor-dependent mechanism that is blocked by the Alzheimer drug memantine.
Early modifications in N-methyl-D-aspartate receptor subunit mRNA levels in an oxygen and glucose deprivation model using rat hippocampal brain slices.
Age-related changes in hypothalamic gonadotropin-releasing hormone and N-methyl-D-aspartate receptor gene expression, and their regulation by oestrogen, in the female rat.
CaMKII-dependent dendrite ramification and spine generation promote spatial training-induced memory improvement in a rat model of sporadic Alzheimer's disease.
Differential alterations in the expression of NMDA receptor subunits following chronic ethanol treatment in primary cultures of rat cortical and hippocampal neurones.
Glutamatergic signaling through the N-methyl-D-aspartate receptor directly activates medial subpopulations of luteinizing hormone-releasing hormone (LHRH) neurons, but does not appear to mediate the effects of estradiol on LHRH gene expression.
Intrauterine growth restriction due to uteroplacental insufficiency decreased white matter and altered NMDAR subunit composition in juvenile rat hippocampi.
Natural oligomers of the Alzheimer amyloid-beta protein induce reversible synapse loss by modulating an NMDA-type glutamate receptor-dependent signaling pathway.
Protective effect of spleen-yin-nourishing recipe on amyloid beta-peptide-induced damage of primarily cultured rat hippocampal neurons and its mechanism.
